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RTN TRH causes prolonged respiratory stimulation

C L Cream1, A Li, E E Nattie

  • 1Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756-0001, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|September 18, 1997
PubMed
Summary

Thyrotropin-releasing hormone (TRH) powerfully stimulates breathing and blood pressure in rats by acting on the retrotrapezoid nucleus. The phrenic response appears specific to TRH receptors.

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Area of Science:

  • Neuroscience
  • Respiratory Physiology
  • Endocrinology

Background:

  • The retrotrapezoid nucleus (RTN) is a key respiratory control center.
  • Thyrotropin-releasing hormone (TRH) is a hypothalamic peptide with diverse physiological roles.

Purpose of the Study:

  • To investigate the effects of TRH and its related compounds on respiratory and cardiovascular functions within the RTN.
  • To determine the specificity of TRH's action on respiratory centers.

Main Methods:

  • Direct microinjections of TRH, TRHOH, and cHP into the RTN of anesthetized rats.
  • Monitoring of phrenic nerve activity (Phr . f), phrenic amplitude (Phr), respiratory frequency (f), and blood pressure.
  • Anatomic verification of injection sites.

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Main Results:

  • TRH dose-dependently increased Phr . f, Phr, f, and blood pressure, with significant effects at higher doses (1.0-10 mM).
  • Stimulation by TRH reached 150% of baseline and lasted up to 270 minutes.
  • TRHOH and cHP increased respiratory frequency (f) but did not affect phrenic amplitude (Phr), suggesting a non-specific effect on f.

Conclusions:

  • TRH exerts a potent stimulatory effect on Phr . f within the RTN.
  • The TRH-induced phrenic response appears to be mediated specifically by TRH receptors.
  • The effect of TRH on respiratory frequency may involve non-specific mechanisms.